Biochemical Genetics最新文献_第8页

ZMIZ1 Regulates Proliferation, Autophagy and Apoptosis of Colon Cancer Cells by Mediating Ubiquitin-Proteasome Degradation of SIRT1. ZMIZ1通过介导SIRT1的泛素-蛋白酶体降解调控结肠癌细胞的增殖、自噬和凋亡

IF 2.1 4区生物学

Biochemical Genetics Pub Date : 2024-08-01 Epub Date: 2024-01-12 DOI: 10.1007/s10528-023-10573-9

Min Huang, Junfeng Wang, Zhengrong Zhang, Xueliang Zuo

{"title":"ZMIZ1 Regulates Proliferation, Autophagy and Apoptosis of Colon Cancer Cells by Mediating Ubiquitin-Proteasome Degradation of SIRT1.","authors":"Min Huang, Junfeng Wang, Zhengrong Zhang, Xueliang Zuo","doi":"10.1007/s10528-023-10573-9","DOIUrl":"10.1007/s10528-023-10573-9","url":null,"abstract":"There are nearly 1.15 million new cases of colon cancer, as well as 586,858 deaths from colon cancer worldwide in 2020. The aim of this study is to reveal whether ZMIZ1 can control the fate of colon cancer cells and the mechanism by which it functions. Specific shRNA transfection was used to knock down the expression of ZMIZ1 in colon cancer cell lines (HCT116 and HT29), and cell proliferation was detected using EdU and CCK-8 reagents, apoptosis by flow cytometry, and autophagy by western blot. The interaction of ZMIZ1 and SIRT1 was analyzed. Knockdown of ZMIZ1 significantly inhibited autophagy and proliferation, and induced apoptosis of HCT116 and HT29 cells. The mRNA level of SIRT1 was not affected by ZMIZ1 knockdown, but the protein level of SIRT1 was significantly decreased and the protein level of the SIRT1-specific substrate, acetylated FOXO3a, was reduced. Immunoprecipitation assays identified the interaction between SIRT1 and ZMIZ1 in HCT116 and HT29 cells. ZMIZ1 increased intracellular ubiquitination of SIRT1. Knockdown or pharmacological inhibition of SIRT1 neutralized the effects of ZMIZ knockdown on proliferation, autophagy and apoptosis in HCT116 and HT29 cells. ZMIZ1 may control the fate of colon cancer cells through the SIRT1/FOXO3a axis. Targeting ZMIZ1 would be beneficial for the treatment of colon cancer.","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":"3245-3259"},"PeriodicalIF":2.1,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11289246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139428392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Role of ACE2 Receptor and Its Polymorphisms in COVID-19 Infection and Severity and Its Association with Lipid Profile, Thrombin, and D-Dimer Levels in Iraqi Patients: A Cross-Sectional Study. 伊拉克患者 ACE2 受体及其多态性在 COVID-19 感染和严重程度中的作用及其与血脂概况、凝血酶和 D-Dimer 水平的关系：一项横断面研究

IF 2.1 4区生物学

Biochemical Genetics Pub Date : 2024-07-31 DOI: 10.1007/s10528-024-10890-7

Ban Adnan Hatem, Ferdous A Jabir

{"title":"The Role of ACE2 Receptor and Its Polymorphisms in COVID-19 Infection and Severity and Its Association with Lipid Profile, Thrombin, and D-Dimer Levels in Iraqi Patients: A Cross-Sectional Study.","authors":"Ban Adnan Hatem, Ferdous A Jabir","doi":"10.1007/s10528-024-10890-7","DOIUrl":"https://doi.org/10.1007/s10528-024-10890-7","url":null,"abstract":"COVID-19 patients experience a complex interplay involving ACE2, thrombin, D-dimer, and lipid profile, yet its full understanding remains elusive. ACE2, a pivotal regulator of the renin-angiotensin system and the primary receptor for SARS-CoV-2 undergoes downregulation upon viral binding, potentially leading to severe cases with acute respiratory distress syndrome (ARDS). A specific ACE2 gene polymorphism (rs2285666) may be associated with COVID-19 susceptibility, with the A allele potentially increasing infection risk. COVID-19 disease progression is linked to coagulation abnormalities, but the exact connection with thrombin and D-dimer remains uncertain. A study examining coagulation parameters in COVID-19 patients admitted to Al-Diwania Educational Hospital from February to May 2022 found that thrombin and D-dimer levels were directly related to disease severity. Severe cases exhibited significantly altered coagulation function compared to mild and recovered cases, with notably higher D-dimer levels and elevated thrombin serum concentrations. Moreover, dyslipidemia, particularly low HDL cholesterol, is a prevalent comorbidity in COVID-19 patients and may be linked to worse outcomes. In conclusion, COVID-19 is associated with a prothrombotic state and dysregulation of the renin-angiotensin system due to ACE2 downregulation following viral binding. The intricate interplay between ACE2, thrombin, D-dimer, and lipid profile necessitates further investigation. The multifaceted nature of the disease demands continued research to unravel its pathogenesis and identify potential therapeutic targets.","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141858691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

N₇-Ended Walker PCR: An Efficient Genome-Walking Tool. N7-末端 Walker PCR：一种高效的基因组漫步工具

IF 2.1 4区生物学

Biochemical Genetics Pub Date : 2024-07-30 DOI: 10.1007/s10528-024-10896-1

Bingkun Tian, Hongjing Wu, Rongrong Wang, Hong Chen, Haixing Li

引用次数: 0

ADAM12 Silencing Mediated by FOXC2 Represses Meningioma Progression Through Inactivating the JAK1/STAT3/VEGFA Pathway FOXC2介导的ADAM12沉默通过抑制JAK1/STAT3/VEGFA通路抑制脑膜瘤进展

IF 2.4 4区生物学

Biochemical Genetics Pub Date : 2024-07-27 DOI: 10.1007/s10528-024-10893-4

Huaming Zhang, Bing Yang

{"title":"ADAM12 Silencing Mediated by FOXC2 Represses Meningioma Progression Through Inactivating the JAK1/STAT3/VEGFA Pathway","authors":"Huaming Zhang, Bing Yang","doi":"10.1007/s10528-024-10893-4","DOIUrl":"https://doi.org/10.1007/s10528-024-10893-4","url":null,"abstract":"Meningioma is a prevalently intracranial tumor, and the malignant type is aggressive with high recurrence. A Disintegrin and Metalloprotease 12 (ADAM12) is a common oncogene and differentially expressed in meningioma. However, its roles and mechanisms in meningioma development remain obscure. The differentially expressed genes in meningioma were analyzed by GEO (GSE77259 and GSE43290) datasets and weighted gene co-expression network analysis (WGCNA) based on GSE16581. ADAM12 expression was measured via qRT-PCR and western blot. The correlation between ADAM12 and FOXC2 was predicted through JASPER tool and identified via luciferase reporter analysis. Cell proliferation, migration and invasion were investigated using CCK-8, EdU, transwell assays. The JAK1/STAT3/VEGFA signaling was activated by IL-6, and analyzed via western blot. The differentially expressed ADAM12 in meningioma was screened by WGCNA and GEO analyses. ADAM12 silencing repressed meningioma cell proliferation, and decreased migration and invasion. The transcription factor FOXC2 expression was enhanced in meningioma based on GSE77259 and GSE43290 datasets, and positively induced ADAM12 transcription. The JAK1/STAT3/VEGFA signaling was inactivated due to ADAM12 silencing and activated via IL-6. Upregulation of FOXC2 promoted cell proliferation, migration and invasion, and these effects were reversed by silencing ADAM12. ADAM12 knockdown mediated via FOXC2 silencing restrained proliferation, migration and invasion of meningioma cells through inactivating the JAK1/STAT3/VEGFA pathway.","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":"40 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141782661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Impact of 5' Near Gene Variants of Mannose Binding Lectin (MBL2) on Breast Cancer Risk. 甘露糖结合凝集素 (MBL2) 5' 附近基因变异对乳腺癌风险的影响。

IF 2.1 4区生物学

Biochemical Genetics Pub Date : 2024-07-26 DOI: 10.1007/s10528-024-10894-3

Shreya Singh Kashyap, Surmeet Kaur, Rajiv Kumar Devgan, Sumitoj Singh, Jatinder Singh, Manpreet Kaur

{"title":"Impact of 5' Near Gene Variants of Mannose Binding Lectin (MBL2) on Breast Cancer Risk.","authors":"Shreya Singh Kashyap, Surmeet Kaur, Rajiv Kumar Devgan, Sumitoj Singh, Jatinder Singh, Manpreet Kaur","doi":"10.1007/s10528-024-10894-3","DOIUrl":"https://doi.org/10.1007/s10528-024-10894-3","url":null,"abstract":"The immune system plays a bifaceted role in tumour development through modulation of inflammation. MBL binds to damage-associated molecular patterns and induces inflammation through the activation of complement pathway. Dysregulated inflammation plays a major role in breast cancer pathogenesis, thereby suggesting its contribution towards breast cancer risk. Literature asserts single-nucleotide polymorphisms (SNPs) modulating serum MBL levels. Therefore, studying MBL2 SNPs in breast cancer might provide valuable insight in the disease pathogenesis. The present case-control association study aimed to elucidate the association between MBL2 5' near gene SNPs and breast cancer risk. Breast cancer patients were recruited from Government Medical College, G.N.D. Hospital, Amritsar. The age- and gender-matched genetically unrelated healthy individuals, from adjoining regions, with no history of malignancy up to three generations were recruited as controls. The SNPs of MBL2 from the 5' near gene region with putative functional significance were selected based upon the in silico analysis and literature review. The genotypic, allelic and haplotype frequencies for the studied variants were assessed and compared in the study participants by ARMS-PCR and PCR-RFLP. No difference in allelic, genotypic and haplotype frequencies was reported for rs7096206, rs7084554 and rs11003125 in both the participant groups. rs7084554 (CC) was found to confer risk towards hormone receptor-positive breast cancer. An intermediate LD was observed between rs7084554 and rs11003125. The study reports association between MBL2 variant (rs7084554) and hormone receptor-positive breast cancer risk. Further research in this direction might validate the findings.","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141764764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Platelet-Rich Plasma (PRP) Mitigates Kidney Dysfunction in Alloxan-Induced Diabetic Mice via Modulation of Renal Iron Regulatory Genes. 富血小板血浆 (PRP) 通过调节肾脏铁调节基因缓解阿脲诱导糖尿病小鼠的肾功能障碍

IF 2.1 4区生物学

Biochemical Genetics Pub Date : 2024-07-26 DOI: 10.1007/s10528-024-10871-w

Humaira Allay Ali, Muddasir Hassan Abbasi, Tasleem Akhtar, Amin Arif, Mehreen Anjum, Sana Fatima, Rabia Mehmood, Adil Farooq, Nadeem Sheikh, Muhammad Babar Khawar

{"title":"Platelet-Rich Plasma (PRP) Mitigates Kidney Dysfunction in Alloxan-Induced Diabetic Mice via Modulation of Renal Iron Regulatory Genes.","authors":"Humaira Allay Ali, Muddasir Hassan Abbasi, Tasleem Akhtar, Amin Arif, Mehreen Anjum, Sana Fatima, Rabia Mehmood, Adil Farooq, Nadeem Sheikh, Muhammad Babar Khawar","doi":"10.1007/s10528-024-10871-w","DOIUrl":"https://doi.org/10.1007/s10528-024-10871-w","url":null,"abstract":"Kidney dysfunction is a prevalent complication of diabetes mellitus, contributing significantly to diabetes-related morbidity and mortality. We aim to explore whether platelet-rich plasma administration can modulate iron regulation mechanism within the kidney, thereby mitigating renal dysfunction associated with diabetes. Albino mice with an average body weight of 20 ± 5 g were randomly divided into five groups (N = 50; n = 10): Control Group, PRP Group, diabetic group (DG), treated group A (TA), and treated group B (TB). A single intraperitoneal dose of alloxan (160 mg/kg of body weight) was administered to mice in the DG and in both treated groups. Upon confirmation of diabetes, the DG was left untreated, while PRP treatment (0.5 ml/kg of body weight) was administered to the TA and TB groups for two and four weeks, respectively. Histological examinations of kidney tissues revealed notable signs of damage in DG, which were subsequently improved upon PRP treatment. Likewise, PRP treatment restored the changes in liver enzymes, oxidative stress biomarkers and serum electrolytes in both treated groups. Furthermore, there was an observed upregulation of iron regulatory genes, such as Renin, Epo, Hepc, Kim1, and Hfe, in the DG, accompanied by a downregulation of Tfr1 and Fpn; however, Dmt1 and Dcytb1 expression remained unaltered. Treatment with PRP restored the expression of iron regulatory genes in both treated groups. This study concluded that PRP treatment effectively restored the renal histochemistry and the expression of renal iron regulatory genes in an alloxan-induced diabetic mice model.","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141764765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Familial Episodic Pain Syndrome: A Japanese Family Harboring the Novel Variant c.2431C>T (p.Leu811Phe) in SCN11A. 家族性发作性疼痛综合征：一个携带 SCN11A 变异 c.2431C>T (p.Leu811Phe) 的日本家庭。

IF 2.1 4区生物学

Biochemical Genetics Pub Date : 2024-07-25 DOI: 10.1007/s10528-024-10888-1

Chioko Nagao, Hiroko Okuda, Gert-Jan Bekker, Atsuko Noguchi, Tsutomu Takahashi, Akio Koizumi, Shohab Youssefian, Tohru Tezuka, Shinji Akioka

{"title":"Familial Episodic Pain Syndrome: A Japanese Family Harboring the Novel Variant c.2431C>T (p.Leu811Phe) in SCN11A.","authors":"Chioko Nagao, Hiroko Okuda, Gert-Jan Bekker, Atsuko Noguchi, Tsutomu Takahashi, Akio Koizumi, Shohab Youssefian, Tohru Tezuka, Shinji Akioka","doi":"10.1007/s10528-024-10888-1","DOIUrl":"https://doi.org/10.1007/s10528-024-10888-1","url":null,"abstract":"Familial episodic pain syndrome (FEPS) is an autosomal-dominant inherited disorder characterized by paroxysmal pain episodes. FEPS appears in early childhood, gradually disappearing with age, and pain episodes can be triggered by fatigue, bad weather, and cold temperatures. Several gain-of-function variants have been reported for SCN9A, SCN10A, or SCN11A, which encode the voltage-gated sodium channel α subunits Nav1.7, Nav1.8, and Nav1.9, respectively. In this study, we conducted genetic analysis in a four-generation Japanese pedigree. The proband was a 7-year-old girl, and her brother, sister, mother, and grandmother were also experiencing or had experienced pain episodes and were considered to be affected. The father was unaffected. Sequencing of SCN9A, SCN10A, and SCN11A in the proband revealed a novel heterozygous variant of SCN11A: g.38894937G>A (c.2431C>T, p.Leu811Phe). This variant was confirmed in other affected members but not in the unaffected father. The affected residue, Leu811, is located within the DII/S6 helix of Nav1.9 and is important for signal transduction from the voltage-sensing domain and pore opening. On the other hand, the c.2432T>C (p.Leu811Pro) variant is known to cause congenital insensitivity to pain (CIP). Molecular dynamics simulations showed that p.Leu811Phe increased the structural stability of Nav1.9 and prevented the necessary conformational changes, resulting in changes in the dynamics required for function. By contrast, CIP-related p.Leu811Pro destabilized Nav1.9. Thus, we speculate that p.Leu811Phe may lead to current leakage, while p.Leu811Pro can increase the current through Nav1.9.","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

XRCC2 knockdown effectively sensitizes esophageal cancer to albumin-paclitaxel in vitro and in vivo. 在体外和体内敲除 XRCC2 能有效提高食管癌对白蛋白-紫杉醇的敏感性。

IF 2.1 4区生物学

Biochemical Genetics Pub Date : 2024-07-24 DOI: 10.1007/s10528-024-10885-4

Jia Xu, Xiaoyuan Liu, Zebo Huang, Tingxun Lu, Ying Zhang, Dongyan Cai, Xia Li

{"title":"XRCC2 knockdown effectively sensitizes esophageal cancer to albumin-paclitaxel in vitro and in vivo.","authors":"Jia Xu, Xiaoyuan Liu, Zebo Huang, Tingxun Lu, Ying Zhang, Dongyan Cai, Xia Li","doi":"10.1007/s10528-024-10885-4","DOIUrl":"https://doi.org/10.1007/s10528-024-10885-4","url":null,"abstract":"Esophageal cancer (EC), a prevalent malignancy, has a high incidence and mortality. X-ray repair cross complementing 2 (XRCC2) functions on DNA damage and repair that works the progression of various cancers. Nevertheless, the role and mechanism of XRCC2 remain unknown in EC. The XRCC2 expression was examined by reverse transcription quantitative polymerase chain reaction and western blot. The function of XRCC2 in EC were investigated through cell counting kit-8, colony formation, transwell, flow cytometry, chromatin immunoprecipitation, luciferase, and western blot experiments. Besides, the role of XRCC2 in EC was assessed by western blot and immunohistochemistry experiments after nude mice were injected with EC109 cells and treated with nab-paclitaxel. The XRCC2 expression was upregulated in EC. Knockdown of XRCC2 diminished cell viability, and the number of colonies, migration cells and invasion cells of KYSE150 and EC109 cells. Silencing of XRCC2 diminished the cell viability of both two cells with a lower IC50, whereas boosted the apoptosis rate of both cells with the treatment of albumin-paclitaxel. All these outcomes were reverse with the upregulation of XRCC2 in both two cells. Mechanically, XRCC2 was transcriptionally regulated by specificity protein 1 (SP1), and silencing of SP1 inhibited the cell growth of EC. In vivo, transfection of shXRCC2 with or without albumin-paclitaxel treatment both decreased the tumor size and weight, as well as the expression of XRCC2 and Ki-67 in xenografted mice. XRCC2 transcriptionally regulated by SP2 promoted proliferation, migration, invasion, and chemoresistance of EC cells.","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HTR3A Promotes Non-small Cell Lung Cancer Through the FOXH1/Wnt3A Signaling Pathway. HTR3A 通过 FOXH1/Wnt3A 信号通路促进非小细胞肺癌的发生

IF 2.1 4区生物学

Biochemical Genetics Pub Date : 2024-07-24 DOI: 10.1007/s10528-024-10872-9

Zeqin Wu, Jiufei Li, Minglian Zhong, Zhiyuan Xu, Mulan Yang, Chenyang Xu

{"title":"HTR3A Promotes Non-small Cell Lung Cancer Through the FOXH1/Wnt3A Signaling Pathway.","authors":"Zeqin Wu, Jiufei Li, Minglian Zhong, Zhiyuan Xu, Mulan Yang, Chenyang Xu","doi":"10.1007/s10528-024-10872-9","DOIUrl":"https://doi.org/10.1007/s10528-024-10872-9","url":null,"abstract":"5-Hydroxytryptamine receptors (5-HTRs) are strongly correlated with tumor progression in various types of cancer. Despite this, the underlying mechanisms responsible for the role of 5-HTRs in non-small cell lung cancer (NSCLC) remains unclear. This study aimed to investigate the relationship between 5-hydroxytryptamine receptor 3A (HTR3A) and NSCLC development. Our findings indicated a higher distribution of HTR3A expression in NSCLC tissues when compared with normal tissues, where patients with high HTR3A levels demonstrated shorter overall survival times. In vitro analyses revealed that overexpression of HTR3A facilitated the proliferation and migration of NSCLC cell lines (A549 and NCI-H3255). Similarly, a notable acceleration of tumor growth and enhanced pulmonary tumorigenic potential were observed in HTR3A-overexpressing tumor-bearing mice. Mechanistically, upregulation of Forkhead Box H1 (FOXH1) by HTR3A led to the activation of Wnt3A/β-catenin signaling pathways, thereby promoting the development of NSCLC. Our report thus highlights the significance of the HTR3A/FOXH1 axis during tumor progression in NSCLC, proposing HTR3A as a possible diagnostic indicator and candidate target for clinical therapy.","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141750790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of N6-Methyladenosine-Associated lncRNAs and Analysis of Prognostic Signature in Breast Cancer. N6-甲基腺苷相关lncRNA的鉴定及乳腺癌预后特征的分析

IF 2.1 4区生物学

Biochemical Genetics Pub Date : 2024-07-23 DOI: 10.1007/s10528-024-10889-0

Yun Gu, Min Xu, Wangfei Wu, Zhifang Ma, Weiguang Liu

{"title":"Identification of N6-Methyladenosine-Associated lncRNAs and Analysis of Prognostic Signature in Breast Cancer.","authors":"Yun Gu, Min Xu, Wangfei Wu, Zhifang Ma, Weiguang Liu","doi":"10.1007/s10528-024-10889-0","DOIUrl":"https://doi.org/10.1007/s10528-024-10889-0","url":null,"abstract":"Breast cancer represents the predominant malignant neoplasm in women, posing significant threats to both life and health. N6-methyladenosine (m6A) methylation, the most prevalent RNA modification, plays a crucial role in cancer development. This study aims to delineate the prognostic implications of m6A-associated long non-coding RNAs (m6AlncRNAs) and identify potential m6AlncRNA candidates as novel therapeutic targets for breast cancer. Through univariate Cox, Least Absolute Shrinkage and Selection Operator and multiple Cox regression analysis, m6AlncRNA was analyzed and a risk-prognosis model was constructed. Kaplan-Meier analysis, principal component analysis and nomogram were used to evaluate the risk model. Finally, we screened candidate lncRNAs and validated them in breast cancer cell lines. m6AlncRNAs were stratified into three subtypes, and their associations with survival outcomes and immune infiltrating capacities were systematically analyzed. Subsequently, breast cancer patients were stratified into high and low-risk groups based on median risk scores, revealing distinct clinical characteristics, tumor immunoinvasive profiles, tumor mutation burden, and survival probabilities. Additionally, a prognostic model was established, highlighting three promising candidate lncRNAs: ECE1-AS1, NDUFA6-DT, and COL4A2-AS1. This study investigated the prognostic implications of m6A-associated long non-coding RNAs (m6AlncRNAs) and developed a prognostic risk model to identify three potential m6AlncRNA candidates. These findings provide valuable insights into the potential application of these m6AlncRNAs in guiding immunotherapeutic strategies for breast cancer.","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141747071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0